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Stimulating effect of excess iron feeding on spontaneous lung tumor promotion in mice.

Abstract
This study was undertaken to estimate if dietary iron could stimulate factors which promote spontaneous lung tumorigenesis in A/J mice, by measuring biochemical parameters of oxidative stress on pulmonary nuclei, ornithine decarboxylase (ODC) and spermidine/spermine N1-acetyltransferase (SAT) activities as markers of tumor promotion. Feeding excessive iron (500%) to A/J mice for 28 weeks significantly elevated pulmonary DNA single strand break (DNA-SSB) as well as nuclear thiobarbituric acid reactive substances (TBARS) in connection with the increase of nuclear nonheme iron level. In contrast, nuclear alpha-tocopherol levels in the iron-loaded group significantly decreased as compared to that in the control group. Pulmonary ODC and SAT activities showed increasing tendency on feeding excess iron for 28 weeks. These results suggest that dietary iron stimulates spontaneous lung tumor promotion in A/J mice, partly due to the enhancement of oxidative damage to the pulmonary nuclei.
AuthorsT Yano, Y Obata, Y Yano, S Otani, T Ichikawa
JournalInternational journal for vitamin and nutrition research. Internationale Zeitschrift fur Vitamin- und Ernahrungsforschung. Journal international de vitaminologie et de nutrition (Int J Vitam Nutr Res) Vol. 65 Issue 2 Pg. 127-31 ( 1995) ISSN: 0300-9831 [Print] Switzerland
PMID7591532 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Biomarkers, Tumor
  • DNA, Neoplasm
  • Thiobarbituric Acid Reactive Substances
  • Iron
  • Acetyltransferases
  • diamine N-acetyltransferase
  • Ornithine Decarboxylase
Topics
  • Acetyltransferases (analysis)
  • Administration, Oral
  • Animals
  • Biomarkers, Tumor (analysis)
  • Cell Nucleus (chemistry)
  • DNA, Neoplasm (analysis)
  • Diet
  • Dose-Response Relationship, Drug
  • Incidence
  • Iron (administration & dosage, toxicity)
  • Lung (chemistry, enzymology, pathology)
  • Lung Neoplasms (chemically induced, enzymology, epidemiology)
  • Male
  • Mice
  • Mice, Inbred A
  • Ornithine Decarboxylase (analysis)
  • Oxidative Stress
  • Thiobarbituric Acid Reactive Substances (analysis)
  • Time Factors

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